Ali Khavanin
, Ahmad Mohajerian, Alireza Rafati Navaei
* 1 Department of Emergency Medicine, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Abstract
Burn injuries trigger a profound systemic inflammatory response marked by the excessive release of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6), into the bloodstream. These cytokines play pivotal roles as mediators of inflammation, orchestrating complex cellular and molecular events that have widespread effects on various organs, particularly the kidneys. Elevated levels of these inflammatory mediators are strongly implicated in the onset of systemic inflammatory response syndrome (SIRS), a condition characterized by extensive inflammation that can severely impair renal function. Likewise, TNF-α, among these cytokines, has been shown to induce renal vasoconstriction, which reduces renal blood flow and diminishes the glomerular filtration rate. This vasoconstriction leads to renal ischemia, which aggravates damage to tubular epithelial cells, thereby heightening the risk of acute kidney injury (AKI) following burn trauma. Simultaneously, IL-1 and IL-6 contribute to endothelial dysfunction by increasing vascular permeability, facilitating the extravasation of plasma components into interstitial spaces. This fluid shift results in hypovolemia and a decrease in effective circulating blood volume, further compromising renal perfusion. Taken together, these cytokine-driven mechanisms create a vicious cycle of inflammation, vascular dysfunction, and renal injury. Understanding the roles of TNF-α, IL-1, and IL-6 in modulating renal hemodynamics and promoting tubular injury provides critical insights for developing targeted therapeutic strategies aimed at mitigating AKI in burn patients. Effective management of this inflammatory cascade is essential to improve renal outcomes and overall survival in individuals suffering severe burn injuries.